Venous thromboembolism (VTE) is common and life-threatening in patients with lung cancer. Management of VTE is critical for patients with lung cancer. Risk assessment, thromboprophylaxis and treatment of VTE constitute the core issues of VTE management in patients with lung cancer. Although its overall principles should follow recommendations in authoritative guidelines, VTE management in patients with lung cancer may be slightly special in some specific aspects. Despite the extensive validation of Khorana score for patients with all cancer types, its value in VTE risk assessment of patients with lung cancer is controversial. It is important to determine the VTE risk assessment score that can accurately and specifically assess the VTE risk of patients with lung cancer. Clinical practice patterns of thromboprophylaxis may vary by cancer types, since different sites of cancer may have different levels of VTE risk. To understand the thromboprophylaxis specific for lung cancer is of vital importance for patients with lung cancer. Although it is essential to comply with authoritative guidelines, the duration and timing of initiation of thromboprophylaxis in surgical patients with lung cancer may need further study. Taken together, the purpose of this review is to provide an overview of state-of-the-art VTE stewardship specific for patients with lung cancer.

Background: Compared with a lower neutrophil to lymphocyte ratio(NLR), a higher one denotes severe asthma exacerbation in hospitalized asthmatic children. In addition, NLR is significantly higher in pediatric patients with community-acquired pneumonia (CAP) than those without. Nevertheless, its role in pediatric patients with concomitant asthmatic exacerbation and CAP remains unknown. Methods: In this retrospective study including 1032 pediatric patients aged 5 to 14 years old, the diagnostic and prognostic value of NLR in children with concomitant asthmatic exacerbation and non-severe CAP were investigated. Results: The sensitivity and specificity of NLR for a diagnosis of CAP in patients with asthmatic exacerbation were 56.9% and 90.1%, respectively. The cutoff value of NLR for a diagnosis of CAP in patients with asthmatic exacerbation was 4.15 (P < 0.001). The cumulative asthmatic exacerbation during 3-month followup of patients with high NLR were 23 (21.3%) and 58 (42.0%) in the asthma and asthmatic CAP groups, respectively (P < 0.001). The patients with high NLR who had unimproved CAP were 15 (8.3%) and 23 (12.2%) in the CAP and asthmatic CAP groups, respectively (P = 0.006). Multivariate analyses showed that along with the increase of NLR by 1.0 point, the HR for the occurrence of asthmatic exacerbation and unimproved CAP were 2.91 [1.83–3.96] (P = 0.001) and 3.38 [1.66–5.10] (P < 0.001), respectively. Conclusions: NLR had high and moderate diagnostic value for the exclusion and indication of CAP, respectively, in pediatric patients with asthmatic exacerbation. It also had prognostic value for the outcomes of pediatric patients with concomitant asthmatic exacerbation and CAP.

Background: For critically ill patients in the intensive care unit (ICU), acute respiratory failure (ARF) stands as a prominent cause of mortality. Anion gap (AG) denotes the disparity between unmeasured cations and anions. Adjusting AG for albumin levels results in the albumin corrected anion gap (ACAG), which provides a more accurate representation of the body's acid–base status. Elevated ACAG may arise from ARF‐induced cellular hypoxia and metabolic acidosis. However, limited research has investigated the association between ACAG and the 28‐day all‐cause mortality of ARF patients in critical care.Methods: Using the Medical Information Mart for Intensive Care (MIMIC‐IV 2.2) database, a retrospective data analysis was conducted, specifically targeting critically ill patients diagnosed with ARF. Serum ACAG was collected within 24 hours of the patient's admission to the ICU. The association between ACAG levels and 28‐day all‐cause mortality was investigated using smooth curve fitting, a multivariate Cox proportional hazard regression model, and Kaplan–Meier survival curve analysis. Furthermore, the consistency of these relationships was assessed through interaction and subgroup analyses.Results: The study involved the enrollment of 3888 eligible participants in total. After adjusting for confounding variables in the multivariable Cox regression analysis model, we noticed a positive linear relationship between the ACAG value and the ICU's 28‐day all‐cause mortality rate. When ACAG was used as a continuous variable, a 3.1% increase in 28‐day all‐cause mortality was associated with a 1.0‐mmol/L increase in ACAG (adjusted HR = 1.037, 95% CI: 1.025–1.048, p < 0.001). In the 28‐day all‐cause mortality, the highest and intermediate ACAG groups (adjusted HR 1.483, 95% CI: 1.244–1.768 and adjusted HR 1.244, 95% CI: 1.062–1.457, respectively) were notably higher than the lowest ACAG group when ACAG was utilized as a tertiles categorical variable. The substantial association between ACAG and 28‐day all‐cause mortality in the ICU was consistently demonstrated through subgroup analysis.Conclusions: Among ICU patients with ARF, an elevated ACAG is linked to an elevated risk of 28‐day all‐cause mortality. There exists a linearly positive relationship between the 28‐day all‐cause mortality and ACAG.

Background Occurrence of chronic thromboembolic disease (CTED) after 3 or 6 months of standard and effective anticoagulation is not uncommon in patients with acute pulmonary embolism (PE). To date, there has been no scoring model for the prediction of CTED occurrence. Methods A Prediction Rule for CTED (PRC) was established in the establishment cohort (n=1,124) and then validated in the validation cohort (n=211). Both original and simplified versions of the PRC score were provided by using different scoring and cut-offs. Results The PRC score included 10 items: active cancer (3.641; 2.338-4.944; p 30 kg/m2 (2.186; 1.573-2.799; p=0.001), chronic immobility (2.135; 1.741-2.529; p=0.001), D-dimer > 2,000 ng/mL (1.618; 1.274-1.962; p=0.005), PE with deep vein thrombosis (3.199; 2.356-4.042; p<0.001), previous venous thromboembolism (VTE) history (5.268; 3.472-7.064; p<0.001), thromboembolism besides VTE (4.954; 3.150-6.758; p<0.001), thrombophilia (3.438; 2.573-4.303; p<0.001), and unprovoked VTE (2.227; 1.471-2.983; p=0.001). In the establishment cohort, the sensitivity, specificity, Youden index (YI), and C-index were 85.5%, 79.7%, 0.652, and 0.821 (0.732-0.909) when using the original PRC score, whereas they were 87.9%, 74.6%, 0.625, and 0.807 (0.718-0.897) when using the simplified one, respectively (Kappa coefficient 0.819, p-value of McNemar's test 0.786). In the validation cohort, the sensitivity, specificity, YI, and C-index were 86.3%, 76.3%, 0.626, and 0.815 (0.707-0.923) when using the original PRC score, whereas they were 85.0%, 78.6%, 0.636, and 0.818 (0.725-0.911) when using the simplified one, respectively (Kappa coefficient 0.912, p-value of McNemar's test 0.937); both were better than that of the DASH score (72.5%, 69.5%, 0.420, and 0.621 [0.532-0.710]). Conclusions A prediction score for CTED occurrence, termed PRC, predicted the likelihood of CTED occurrence after 3 or 6 months of standard anticoagulation in hospitalised patients with a diagnosis of acute PE.